Human cartilage homogenates influence the crystallization of monosodium urate (MSU) and the inflammatory response to MSU crystals: a potential link between osteoarthritis and gout.

Monosodium urate (MSU) crystal deposition and gout flares frequently affect osteoarthritic joints. This study examined the effects of human cartilage homogenates on MSU crystallization and MSU crystal-induced inflammation.Human cartilage homogenates were prepared from macroscopically-healthy and macroscopically-diseased knee joint samples. Crystallization assays were used to test the effects of cartilage homogenates or individual cartilage factors on MSU crystallization. Changes in urate solubility, crystal nucleation, crystal growth, and total crystal mass were determined. THP-1 cell assays were used to assess cytokine release following culture with MSU crystals grown in the presence or absence of cartilage homogenates or individual proteins.Addition of 5% and 10% healthy cartilage homogenate increased the total mass of MSU crystals formed and resulted in formation of shorter MSU crystals, compared to no cartilage. MSU crystal bows were observed in the presence and absence of cartilage homogenates; however, bows formed in the presence of cartilage homogenates were significantly shorter than control bows. There were no differences between macroscopically-healthy cartilage and macroscopically-diseased cartilage homogenates in all assessments. Type II collagen and albumin also led to the formation of shorter MSU crystals. In THP-1 cell assays, MSU crystals grown with healthy cartilage homogenate increased release of interleukin-8; whereas MSU crystals grown with type II collagen or albumin did not.In the presence of elevated urate, human cartilage homogenates increase MSU crystal formation and promote the formation of smaller crystals which have greater inflammatory potential. These processes may contribute to the predilection of gout to osteoarthritic joints. This article is protected by copyright. All rights reserved.